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Circadian Rhythm Disturbances in Mood Disorders: Insights into the Role of the Suprachiasmatic Nucleus

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Vadnie, Chelsea A., McClung, Colleen A.·2017·Neural Plasticity
DOI 10.1155/2017/1504507PMC PMC5694588
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Abstract

Circadian rhythm disturbances are a common symptom among individuals with mood disorders. The suprachiasmatic nucleus (SCN), in the ventral part of the anterior hypothalamus, orchestrates physiological and behavioral circadian rhythms. The SCN consists of self-sustaining oscillators and receives photic and nonphotic cues, which entrain the SCN to the external environment. In turn, through synaptic and hormonal mechanisms, the SCN can drive and synchronize circadian rhythms in extra-SCN brain regions and peripheral tissues. Thus, genetic or environmental perturbations of SCN rhythms could disrupt brain regions more closely related to mood regulation and cause mood disturbances. Here, we review clinical and preclinical studies that provide evidence both for and against a causal role for the SCN in mood disorders.

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Figure 1 Inputs and outputs of the suprachiasmatic nucleus (SCN). (a) The main inputs to the SCN come from the intrinsically photosensitive retinal ganglion cells (ipRGCs), median raphe (MnR), and intergeniculate leaflet (IGL) (as reviewed in [38]). The retinohypothalamic tract (RHT) originates from ipRGCs and primarily terminates in the SCN. The RHT terminals release glutamate (Glu) and pituitary adenylate cyclase-activating polypeptide, which entrain the SCN to the light-dark cycle [379, 380]. ipRGCs also project to the IGL [381]. The pathway from the IGL to the SCN is called the geniculohypothalamic tract (GHT). GHT terminals release GABA and neuropeptide Y onto the SCN (as reviewed in [382]). GHT relays photic and nonphotic information to the SCN. The SCN also receives input from midbrain raphe nuclei, directly from the MnR and indirectly from the dorsal raphe (DR) through the IGL [383]. Serotonergic (5HT) signaling in the SCN modulates the effects of photic cues and plays a major role in the effects of nonphotic cues [130, 131]. (b) The SCN projects to other areas of the hypothalamus, including the paraventricular nucleus (PVN), dorsomedial nucleus (DMH), and the medial preoptic area (MPOA) (as reviewed in [38]). The SCN also directly projects to areas outside of the hypothalamus, such as the paraventricular nucleus of the thalamus (PVT), septum (Sptm), and lateral habenula (LHb). The SCN indirectly projects to the ventral tegmental area (VTA), locus coeruleus (LC), and DR [38, 43].
Figure 1 Inputs and outputs of the suprachiasmatic nucleus (SCN). (a) The main inputs to the SCN come from the intrinsically photosensitive retinal ganglion cells (ipRGCs), median raphe (MnR), and intergeniculate leaflet (IGL) (as reviewed in [38]). The retinohypothalamic tract (RHT) originates from ipRGCs and primarily terminates in the SCN. The RHT terminals release glutamate (Glu) and pituitary adenylate cyclase-activating polypeptide, which entrain the SCN to the light-dark cycle [379, 380]. ipRGCs also project to the IGL [381]. The pathway from the IGL to the SCN is called the geniculohypothalamic tract (GHT). GHT terminals release GABA and neuropeptide Y onto the SCN (as reviewed in [382]). GHT relays photic and nonphotic information to the SCN. The SCN also receives input from midbrain raphe nuclei, directly from the MnR and indirectly from the dorsal raphe (DR) through the IGL [383]. Serotonergic (5HT) signaling in the SCN modulates the effects of photic cues and plays a major role in the effects of nonphotic cues [130, 131]. (b) The SCN projects to other areas of the hypothalamus, including the paraventricular nucleus (PVN), dorsomedial nucleus (DMH), and the medial preoptic area (MPOA) (as reviewed in [38]). The SCN also directly projects to areas outside of the hypothalamus, such as the paraventricular nucleus of the thalamus (PVT), septum (Sptm), and lateral habenula (LHb). The SCN indirectly projects to the ventral tegmental area (VTA), locus coeruleus (LC), and DR [38, 43].CC BY · PubMed Central
Figure 2 Potential mechanisms underlying the associations between circadian rhythm disruptions and mood disorders. Seasonal changes, jet lag, and shift work may disturb mood in vulnerable individuals through projections from intrinsically photosensitive retinal ganglion cells (ipRGCs) directly to mood-related brain regions, or to the suprachiasmatic nucleus (SCN). Alternatively, other environmental insults (e.g., stress) and genetic disturbances (e.g., circadian gene mutations) can affect mood-related brain regions and SCN function. The SCN may disturb mood by directly or indirectly affecting the function of brain regions more closely tied to mood regulation, explaining how circadian rhythm disturbances could affect mood. Conversely, environmental and genetic factors may influence the SCN and mood-related brain regions independently, explaining how circadian rhythm disturbances could be a noncausal symptom of mood disorders.
Figure 2 Potential mechanisms underlying the associations between circadian rhythm disruptions and mood disorders. Seasonal changes, jet lag, and shift work may disturb mood in vulnerable individuals through projections from intrinsically photosensitive retinal ganglion cells (ipRGCs) directly to mood-related brain regions, or to the suprachiasmatic nucleus (SCN). Alternatively, other environmental insults (e.g., stress) and genetic disturbances (e.g., circadian gene mutations) can affect mood-related brain regions and SCN function. The SCN may disturb mood by directly or indirectly affecting the function of brain regions more closely tied to mood regulation, explaining how circadian rhythm disturbances could affect mood. Conversely, environmental and genetic factors may influence the SCN and mood-related brain regions independently, explaining how circadian rhythm disturbances could be a noncausal symptom of mood disorders.CC BY · PubMed Central

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Research works printed but not linked: 12

  1. 1997, Circadian rhythms and depression: clinical and experimental models, 457
  2. 1997, International Journal of Occupational and Environmental Health, 3, S2
  3. 1981, Circadian systems: entrainment
  4. 1983, International Journal of Chronobiology, 8, 129
  5. 1978, Biological Psychiatry, 13, 335
  6. 1984, Biological Psychiatry, 19, 1215
  7. 1997, American Journal of Physiology, 272, 4 part 2, R1178
  8. 1999, American Journal of Physiology, 277, R812
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  10. 2000, Journal of Psychiatry and Neuroscience, 25, 469
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  12. 2007, Neuroendocrinology Letters, 28, 846

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Metadata

Authors
Vadnie, C. A., & McClung, C. A.
Affiliations
University of Pittsburgh (US)
Corresponding author
Vadnie, Chelsea A.
ORCID
Venue
Neural Plasticity
Publisher
Wiley
Published
2017
Volume
2017
Pages
1-28
ISSN
  • 1687-5443 (ISSN-L)
  • 2090-5904
DOI
10.1155/2017/1504507
PMC
PMC5694588
OpenAlex
W2767056255
Cited by
199
References
383
Citations by year
2026: 13 · 2025: 20 · 2024: 25 · 2023: 23 · 2022: 31 · 2021: 29 · 2020: 29 · 2019: 13 · 2018: 15 · 2017: 1
FWCI
1.92
Type
journal article
Language
en
Open access
Licence
Locations
  • Neural Plasticity (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Institutes of Health (DA039865, DA023988, DA037636, MH106460, MH082876)
  • Pfizer (DA039865, DA023988, DA037636, MH106460, MH082876)
  • McKnight Foundation for Neuroscience (DA039865, DA023988, DA037636, MH106460, MH082876)
  • International Mental Health Research Organization (DA039865, DA023988, DA037636, MH106460, MH082876)
  • The Brain and Behavior Foundation (NARSAD) (DA039865, DA023988, DA037636, MH106460, MH082876)
  • National Institute on Drug Abuse (DA039865, DA023988, DA037636, MH106460, MH082876)
  • National Institute of Mental Health (DA039865, DA023988, DA037636, MH106460, MH082876)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
  • Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and related disorders
Keywords
circadian rhythm disruption, mood disorders, suprachiasmatic nucleus, circadian rhythm, mood regulation, circadian clock, hypothalamus
MeSH terms
Animals, Circadian Rhythm, Humans, Neural Pathways, Suprachiasmatic Nucleus, Mood Disorders

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